Conditional inactivation of the E-cadherin gene in thyroid follicular cells affects gland development but does not impair junction formation

Gaetano Calì, Mariastella Zannini, Patrizia Rubini, Carlo Tacchetti, Barbara D'Andrea, Andrea Affuso, Tim Wintermantel, Oreda Boussadia, Daniela Terracciano, Daniel Silberschmidt, Elena Amendola, Mario De Felice, Günther Schütz, Rolf Kemler, Roberto Di Lauro, Lucio Nitsch

Research output: Contribution to journalArticlepeer-review

Abstract

We have conditionally inactivated the E-cadherin gene in the thyroid follicular cells of mouse embryo to unravel its role in thyroid development. We used the Cre-loxP system in which the Cre-recombinase was expressed under the control of the tissue-specific thyroglobulin promoter that becomes active at embryonic d 15. At postnatal d 7, thyroid follicle lumens in the knockout mice were about 30% smaller with respect to control mice and had an irregular shape. E-cadherin was almost completely absent in thyrocytes, β-catenin was significantly reduced, whereas no change in γ-catenin was detected. α-Catenin was also reduced on the cell plasma membrane. Despite the dramatic loss of E-cadherin and β-catenin, cell-cell junctions were not affected, the distribution of tight junction proteins was unaltered, and no increase of thyroglobulin circulating in the blood was observed. In addition, we found that other members of the cadherin family, the R-cadherin and the Ksp-cadherin, were expressed in thyrocytes and that their membrane distribution was not altered in the E-cadherin conditional knockout mouse. Our results indicate that E-cadherin has a role in the development of the thyroid gland and in the expression of β-catenin, but it is not essential for the maintenance of follicular cell adhesion.

Original languageEnglish
Pages (from-to)2737-2746
Number of pages10
JournalEndocrinology
Volume148
Issue number6
DOIs
Publication statusPublished - Jun 2007

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

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